ArticleThe Journal of biological chemistry2019
SRC tyrosine kinase activates the YAP/TAZ axis and thereby drives tumor growth and metastasis.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
115 citing papers in PubMed, 169 citations in OpenAlex.
- Cytotoxic and Anti-Inflammatory Evaluation of Thai Medicinal Plants from Kampramong's Anticancer Remedy Against Upper Respiratory Tract Malignancies.International journal of molecular sciences · 2026Article
- The Imipridone ONC206 Inhibits Tumor Growth and Improves Survival in Patient-Derived Xenograft Models of Uveal Melanoma.Cancers · 2026Article
- Estrogen promotes osteogenesis via YAP1-driven activation of ERα orchestrated through TEAD1 binding to the ERα promoter.Journal of molecular histology · 2026Article
- Membrane Curvature Activates Src kinase and Promotes Metastatic Cancer Cell Survival.bioRxiv : the preprint server for biology · 2026Article
- Mechano-regulation of cancer cell memory in tumor progression and therapy.Mechanobiology in medicine · 2026Review
- Pancreatic cancer: molecular pathogenesis and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Histological fidelity and microenvironmental kinome signatures of metastatic patient-derived organoids.Frontiers in bioengineering and biotechnology · 2026Article
- Extracellular matrix regulates lineage plasticity in prostate cancer through YAP/TEAD.bioRxiv : the preprint server for biology · 2025Article
- The oncogenic potential of YAP requires Y357 phosphorylation in cholangiocytes but not in hepatocytes.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Piezo1-mediated mechanotransduction controls osteocyte maturation and dendrite development via a YAP-CCN-Src signaling axis.Nature communications · 2025Article
- Article
- PTH counteracts Hippo signaling via Src-dependent YAP stabilization to enhance bone marrow stromal cell differentiation.JCI insight · 2025Article
- Drug tolerance and persistence to EGFR inhibitor treatment are mediated by an ILK-SFK-YAP signaling axis in lung adenocarcinoma.Oncogene · 2025Article
- EDA Fibronectin Microarchitecture and YAP Translocation during Wound Closure.ACS biomaterials science & engineering · 2025Article
- [Research Advances in Targeting the YAP/TAZ Signaling Pathway to Improve Cancer Immunotherapy].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Review
- The IGF2BP1 oncogene is a druggable mNAR cancer · 2025Article
- PTPRO represses breast cancer lung metastasis by inhibiting the JAK2-YAP axis.Scientific reports · 2025Article
- Biological and therapeutic implications of sex hormone-related gene clustering in testicular cancer.Basic and clinical andrology · 2025Article
- ASAP1 and ARF1 Regulate Myogenic Differentiation in Rhabdomyosarcoma by Modulating TAZ Activity.Molecular cancer research : MCR · 2025Article
- Enhanced ferroptosis sensitivity promotes the formation of highly myopic cataract via the DDR2-Hippo pathway.Cell death & disease · 2025Article
55 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
When properly employed, targeted therapies are effective cancer treatments. However, the development of such therapies requires the identification of targetable drivers of cancer development and metastasis. The expression and nuclear localization of the transcriptional coactivators Yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) are increased in many human cancers, and experimental evidence indicates that aberrant YAP or TAZ activation drives tumor formation and metastasis. Although these findings make YAP and TAZ appealing therapeutic targets, both have important functions in adult tissues, so directly targeting them could cause adverse effects. The identification of pathways active in cancer cells and required for YAP/TAZ activity could provide a way to inhibit YAP and TAZ. Here, we show that SRC proto-oncogene, nonreceptor tyrosine kinase (SRC) is an important driver of YAP/TAZ activity in human breast cancer and melanoma cells. SRC activation increased YAP/TAZ activity and the expression of YAP/TAZ-regulated genes. In contrast, SRC inhibition or knockdown repressed both YAP/TAZ activity and the expression of YAP/TAZ-regulated genes. We also show that SRC increases the activity of YAP and TAZ by repressing large tumor suppressor homolog (LATS), and we identify the GTPase-activating protein GIT ArfGAP 1 (GIT1) as an SRC effector that regulates both YAP and TAZ. Importantly, we demonstrate that SRC-mediated YAP/TAZ activity promotes tumor growth and enhances metastasis and that SRC-dependent tumor progression depends, at least in part, on YAP and TAZ. Our findings suggest that therapies targeting SRC could help manage some YAP/TAZ-dependent cancers.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.